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Inflammation
| Question | Answer |
|---|---|
| What is inflammation? | Reaction of living tissue to injury. Its a defense mechanism but may be potentially harmful, and is stereotyped regardless of the nature of the injury. In order for inflammation to occur, injury must be non-lethal (Inflammation doesn’t occur after death) |
| What are some normal defense mechanisms of the body? | Lysozyme in tears and urine, Cerumen in ears antibacterial secretions of the skin, mucus/cilia/macrophages of the respiratory system, low pH of the stomach and urine, and most importantly, a complex/effective immune system. |
| What is exudation? | Outpouring of fluids, proteins, and cells from vessels into interstitium or body cavities. Exudate is a extravascular fluid rich in proteins and cells with a specific gravity of greater than 1.020. |
| What does the appearance of exudate signify? | Significant alteration in the normal permeability of small blood vessels in the area of an injury. |
| What is ‘Transudation’? | Outpouring of fluid with little protein (albumin) and a specific gravity of less than 1.012. It is the ultrafiltrate of plasma and it is usually produced in response to hydrostatic imbalance. Permeability is normal. |
| What is Edema? | Excess intracellular fluid – can be exudate or transudate. |
| What is Pus? | Purulent exudate. It is a cell-rich exudate with mainly PMNs and cell debris. It also contains powerful lysozymal enzymes. |
| What are the 5 cardinal signs of inflammation? | 1) Redness, 2) Swelling, 3) Heat, 4) Pain, 5) Loss of function |
| What are the 3 hallmarks of acute inflammation? | Short duration, exudation, and PMNs |
| What are the 4 hallmarks of chronic inflammation? | Longer duration, Lymphocytes, macrophages, and tissue repair |
| Describe the vascular events associated with acute inflammation. | Changes in vascular flow, caliber, and permeability |
| What is the ‘Triple Response of Lewis’? | The 3 hallmark changes in vascular flow and caliber observed in acute inflammation: 1) Pale line after stroke of an inflamed area, 2) Flare, 3) Swelling with blanching |
| What can be seen with the aid of time-lapse microscope during acute inflammation? | 1) Transient vasoconstriction of arterioles = brief/neurogenic, 2) Vasodilation, arterioles first then microcirculation (chemically mediated), 3) Permability change with exudation (chemically mediated), 4) increased viscosity of blood w/ cellular events. |
| What causes the heat and redness associated with inflammation? | Increased blood flow due to vasodilation. |
| What causes the edema and swelling associated with inflammation? | Permeability changes with exudation |
| How are injury and time related in terms of vascular change seen in acute inflammation? | The more severe the injury, the less time is needed for vascular response |
| Describe Starling’s Forces in terms of the increased vascular permeability and leakage seen in acute inflammation. | Fluid moves out of vessels when: Osmotic pressure of interstitial fluid and intravascular hydrostatic pressure increase. Fluid moves into vessels when: Osmotic pressure (increased plasma proteins) intravascularly and tissue hydrostatic pressure increase. |
| What happens to fluid normally pushed into interstitial spaces? | Lymphatics drain it and no edema occurs |
| What increases intravascular hydrostatic pressure? | Vasodilation |
| What decreased intravascular osmotic pressure? | Decrease plasma proteins like albumin |
| Is transudate or exudate associated with the edema cause by vasodilation and decrease of albumin? | Transudate (movement of low protein fluid) |
| Is transudate or exudate associated with leaky endothelium caused by permeability factors (increased vascular permeability) or direct endothelial damage? | Exudate (movement of high protein fluid) = inflammatory edema = hallmark of acute inflammation |
| What is the common factor that normal fluid change depends upon? | intact endothelium |
| What are endothelial cells capable of releasing? | Prostaglandins, Coagulant factor VIII, collagens, and anticoagulant (plasminogen factor) |
| Describe “Immediate transient response”. | Endothelial cell contraction leads to wider intercellular gaps. This process is mediated by histamine. It is reversible, short lived (15-30 minutes), and occurs only in small venules (not capillaries or arterioles) |
| Describe “Junctional retraction”. | TNF and IL-1 mediated process that involves structural reorganization of the cell’s cytoskeleton and disruption of endothelial cell junctions in venules. Occurs 4-6 hours after injury and lasts for 24+ hours. |
| Describe “Immediate Sustained response”. | Direct endothelial injury w/ endothelial cell necrosis and detachment. Occurs in severe injuries such as burns, infections, cuts, and abrasions. Detachment is secondary to platelet adhesion and thrombosis. Begins immediately and persists for hours – days. |
| What is “Delayed Prolonged response”? | Direct injury of endothelial cells by sunburn or endothelial toxins, the response to which begins after 2-12 hours, lasts for hours – days, and involves capillaries and venules. |
| What is “Leukocyte Dependent Endothelial injury”? | Occurs during inflammation, activated inflammatory cells release toxic oxygen species and proteolytic enzymes causing endothelial cell detachment, occurs mostly in venules and pulmonary capillaries = “ICU lung”. Occurs late in the inflammatory process. |
| What is “Increased Transcytosis”? | Occurs in the presence of VEGF and other mediators which increase venular permeability via the vesiculovacuolar intracellular pathway. |
| Are most clinically significant injuries sustained immediately or later? | Immediately |
| What is the most important feature of inflammation? | Accumulation of leukocytes in the affected tissue |
| What do activated leukocytes do? | 1) Engulf, degrade bacteria/immune complexes/cell debris, 2) release lysosomal enzymes, 3) release chemical mediators, 4) release toxic radicals – All of which may help clear inflammation but may also prolong it or increase the injury/damage. |
| What does migration of leukocytes cause, transudate or exudate formation? | Exudate formation |
| What is the the main cellular event during acute inflammation? | Migration of WBCs through vessel walls into adjacent tissue |
| What are the 4 steps, in order, that allow for leukocyte migration? | 1) Margination, 2) Pavementing and Rolling, 3) Adhesion and emigration, and 4) Chemotaxis and Activation |
| Describe Margination. | When blood becomes viscous, theres peripheral orientation of WBCs because of sludging of RBCs (rouleaux formation). Because the chains of RBCs are larger than the leukocytes, the smaller particles get pushed to the periphery near the wall (law of physics) |
| Describe Pavementing and Rolling. | Normally, up to 50% of PMNs are transiently marginating and sticking. During inflammation this % increases as well as the absolute number of PMNs. Rolling and adhesion are the result of adhesion molecules (CAMs) on the leukocyte/endothelial cell surfaces. |
| What are CAMs? | Cell adhesion molecules on the surface of both PMNs and endothelial cells that are either 1) expressed, 2) induced, or 3) enhanced by chemical mediation |
| What are the 4 most important chemotactic factors for PMNs? | 1) Bacterial products, 2) Complement fractions like C5a, 3) Arachidonic acid metabolites like LTB4, and cytokines (chemokines like IL-8) |
| How does a WBC “smell” chemotactic factors? | Specific cell surface receptors for 1) C5a, 2) LTB4, 3) and synthetic olgiopeptides. Receptor binding is rapid, and once it occurs, there is mobilization of membrane-associated Ca2+ which is essential for contractile elements of locomotion. |
| How does WBC locomotion occur? | The pseudopods of WBCs have actin/myosin which is Ca2+ dependent |
| Can chemotactic factor activate leukocytes in addition to promoting their locomotion? | Yes |
| What are the 3 steps involved in phagocytosis? | 1) Recognition and attachment, 2) engulfment, and 3) killing/degradation |
| Describe the Recognition/attachment phase of phagocytosis. | Most often, opsonization via IgG or C3b must occur for microbes to be recognized by phagocytes. The opsins attach to 2 receptors on PMNs/Macrophages = 1) FcyR (for Fc of IgG) or 2) CR1 receptor (for C3b) |
| Describe the engulfment phase of phagocytosis. | Pseudopods extend around microbes with complete enclosure followed by fusion with lysosomes = phagolysosome, during which leakage of enzymes and metabolites (H2O2) leak out of the Phagocyte (“Regurgitation”) causing tissue damage. |
| What happens if a phagocyte is unable to phagocytose and kill a microbe/foreign object? | They get frustrate and lyse, releasing cytotoxic mediators which promote further tissue damage. |
| What is another name for “Frustrated Phagocyte” syndrome? | Reverse endocytosis |
| What does the process of engulfment for phagocytosis require? | Energy, Ca2+, Mg2+. |
| What is the function of the Ca2+ required for the engulfment phase of phagocytosis? | It gets transported across the phagocyte plasma membrane and acts as a second messenger to initiate cell events in microtubules and microfilaments, culminating with engulfment. |
| Which biochemical events are shared by phagocytosis and chemotaxis? | 1) Receptor-ligand binding, 2) phospholipase activation, and 3) eventual increase in Ca2+ in the phagocyte cytosol. |
| CAMs are important for inflammation, but what other process are they involved in? | Cell recognition and adhesion that takes place in the organization of embryonic tissue and organs in the cellular interactions of post-natal life. |
| What are the 2 subtypes of CAMs? | Those which are Ca2+ dependent and those which are not. |
| What type of molecules are involved in ‘rolling’ that are found on phagocytes? | L-selectin on the surface on the surface of phagocytes (PMNs, macrophages, basophils, etc) |
| Describe Leukocyte Adhesion Deficiency. | Lack of Selectins – causes severe infections in which there are no phagocytes present at the site of infection. |
| Which type of molecules are involved in ‘rolling’ that are found in endothelial cells? | E-selectin (ELAM-1) and P-selectin, which can be upregulated by cytokines and function to interact with phagocyte selectins. |
| Which type of molecules are involved in Adhesion and Emigration that are found in endothelial cells? | ICAM-1 (intracellular adhesion molecule) and VCAM-1 (vascular cell adhesion molecule). Both are upregulated during inflammation by various cytokines. |
| What are ‘integrins’? | Transmembrane glycoproteins that are also receptors for ECM. |
| What are the integrin receptors for ICAM-1? | LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18) |
| What are the integrin receptors for VCAM-1? | VLA-4 |
| Do integrin receptors for ICAM-1 and VCAM always adhere whenever they come in contact? | No, these integrins only adhere to their ligands when leukocytes are activated by inflammatory chemotactic factors. |
| What happens when ICAM-1 and VCAM-1 come into contact with their activated integrin receptors? | Phagocytes move between endothelial cell gaps = diapedesis |
| Which type of leukocytes diapedese first? | PMNs, because they are faster and more numerous. Thus they represent the cell type most commonly seen immedatiely after injury occur. Macrophages/Monocytes diapedese later. |
| What is an exception to the rule that PMNs are the first to diapedese to an area of injury/infection? | Viral infections = Lymphocytes diapedese first |
| Define chemotaxis. | unidirectional migration of cells toward an attractant or locomotion oriented along a chemical gradient. |
| What is chemokinesis? | Accelerated random locomotion of cells |
| What cells are the most likely to undergo chemotaxis? | PMNs and Monocytes (this has been proven experimentally with the micropore filter technique of Boyden) |
| Are chemotactic factor exogenous or endogenous? | Can be either |
| What are the two mechanisms for killing/degradation of foreign particles and which is more effective? | Oxygen dependent or non-oxygen dependent – Oxygen dependent killing is most effective (with the H2O2 myeloperoxidase-halide system being the most effective of the 2 oxygen dependent mechansims) |
| Describe oxygen dependent killing of foreign particles. | Burst of oxygen use with an increase in glycogenolysis, increased glucose oxidation (HMP shunt), and production of active oxygen metabolites = 2O2 + NAD(P)H ---> 2O2- + NAD(P)+ + H+ (via NADPH oxidase) |
| How do oxygen metabolites exert their antibacterial properties? | 1) H2O2 myeloperoxidase-halide (Cl-) system = produces HOCl (a powerful oxidant and chlorinator). 2) Myeloperoxidase (MPO) independent killing: H2O2 + O2- ---> OH + OH- + O2 (OH- = potent free radical) |
| What is system is deficient in persons with chronic granulomatous disease of childhood? | Defective H2O2-myeloperoxidase-halide system (deficieny of NADPH oxidase) |
| Describe Oxygen-independent bacteriocidal mechanisms. | H+ ion from increased lactate (carbonic anhydrase action) reduces intravacuolar pH to kill bacteria. Also, Action of substances from WBC granules aid in bacterial killing. Following killing, acid hydrolases degrade dead bacteria within the phagolysosome. |
| What are some bacterial mechanisms to evade phagolysosome-mediated destruction? | Some bacteria simply destroy their captor cell while others (Mycobacterium tuberculosis) live happily within the phagocyte itself (which causes a major problem for eradication of the disease) |
| Monocytes eventually lose their myeloperoxidase (MPO) capabilities during which process? | Transforming into tissue macrophages |
| During phagocytosis, which products do leukocytes release extracellularly and in what ways does this occur? | 1) Lysosomal enzymes, 2) O2 derived metabolites, and 3) Products of arachidonic acid metabolism (prostaglandins, leukotrienes) are lost via: 1) Regurgitation, 2) Reverse endocytosis (frustrated phagocyte syndrome), and 3) cytoxic release (on cell death). |
| Describe the timing of neurogenic mechanisms of mediating inflammation. | These only occur in very early phases of inflammatory reaction (as fleeting episode of vasoconstriction which is followed by anti-dromic reflex of inhibition of vasoconstriction, which contributes to vasoodilation). They are blocked by anesthesia. |
| Does an absence of innervation prevent the very brief neurogenically mediated vasoconstrictive response at the beginning of injury/inflammation? | No, it occurs whether vessels are innervated or not |
| List the 4 cell-derived vasoactive mediators. | 1) Arachidonic acid, 2) Platelet activating factor, 3) Amines (serotonin, histamine), and 4) Endothelins |
| List the 2 plasma-derived vasoactive mediators. | 1) Kinins/Coagulation cascade and 2) Complement cascade |
| Describe vasoactive mediation by arachidonic acid metabolites. | Derived from the plasma membrane’s phospholipids released by phospholipases from lysosomes in response to physical, chemical, and mechanical stimuli. The end products are prostaglandins and leukotrienes. |
| What is the function of leukotrienes? | Increase vascular permeability and have chemotactic activity. |
| What is the function of prostaglandins? | Increase vascular permeability and increase vasodilation. |
| Describe Platelet activating factor (PAF). | Generated by stimulation of inflammatory cells, endothelial cells, and damaged tissue cells = powerful vasodilator, increases permeability, chemotactic (eosinophils), platelet aggregation at site of injury. |
| What inactivates histamine? | Histaminase |
| Which cells produce platelet activating factor (PAF)? | Mast cells and basophils, in response to IgE mediated reactions |
| Describe the vasoactive amine known as Histamine. | Histamine is present in the granules of mast cells, basophils, and platelets. It is a powerful vasodilator and increaser of vascular permeability in venules (only). It acts on H1 receptors and is short lived (30-60 minutes). |
| Which agents are responsible for the release of histamine from *mast cells*? | 1) Physical trauma such as cold exposure, 2) Immunologic reactions (via receptors for IgE), 3) C3a and C5a (anaphylatoxins), 4) Histamine releasing factors from PMNs, monocytes, and platelets, and 5) IL-1 |
| Describe the vasoactive amine known as Serotonin. | Serotonin is found only in platelets. It is a powerful vasodilator and increaser of vascular permeability in venules (only). |
| Which is the more important vasoactive amine in humans, serotonin or histamine? | Histamine |
| What mediates mast cell degranulation on binding of degranulation receptors? | Adenyl-cyclase activation and production of cAMP (Gs mechanism) which moves granules to the cell’s surface |
| Which agents are responsible for the release of histamine and serotonin from *platelets*? | Contact with collagen, 2) thrombin, 3) AFP, 4) Antigen-Antibody complexes, and 5) platelet activating factor (PAF) |
| Describe endothelins. | Peptide produced by endothelial cells which has powerful *vasoconstrictive* power |
| What are the 3 components of the “Plasma Protease Systems”? | 3 different but interrelated systems: 1) Complement cascade, 2) clotting system, 3) kinin system |
| Describe, in general, the actions of the 3 components of the Plasma Protease System. | Series of inactive prozymes converted to activate enzymes via cleavage into 2+ components, the largest of which is the active enzyme which initiates the associated cascade (smaller components = potent biochemical mediators of inflammatory response) |
| Describe the Kinin system. | Hageman factor (XII) ---> Prekallikrein activator (XIIa) by collagen, etc, XIIa activates the coagulation cascade (Prekallibkein ---> Kallibkein, High Molecular Weight Kininogen ---> Bradykinin which causes vasodilation, vascular permeability, and pain) |
| What is the active kinin produced by the kinin cascade? | Bradykinin (causes smooth muscle contraction, vasodilation, increased vascular permability, and pain) which acts on endothelial cells to increase gaps, inactivated by plasma/tissues kininases. |
| When does Bradykinin work, early or late phases of inflammation? | Only in early phases. |
| What mediates pain? | Bradykinin (via irritation of nerve endings) |
| What does the clotting/coagulation system result in? | Fibrinous exudate/meshwork @ inflamed site to trap cells/microbes/foreign bodies. This prevents the spread of infection and inflammation into the surrounding tissues, keeping cell debris, bacteria, and foreign bodies at the site of phagocytic activity. |
| What is the main substance of the meshwork (final product) of the clotting/coagulative system? | Fibrin |
| What are the two branches of the clotting/coagulation cascade? | Intrinsic and Extrinsic pathways |
| What activates the intrinsic clotting/coagulation cascade? | Collagen |
| What activates the extrinsic clotting/coagulation cascade? | Cell injury and its byproducts |
| What is the common factor that links the intrinsic and extrinsic clotting/coagulation pathways? | Factor X |
| What is the common factor that links all 3 Plasma Protease Systems? | Factor XII |
| List the steps in the common clotting/coagulation cascade. | Xa (eventually converts) Va Phospholipid (converts) Prothrombin to Thrombin which converts Fibrinogen to Fibrin and Fibrinopeptide monomers which result in Fibrin polymers. |
| What is the function of the low molecular weight fibrino-peptides released from fibrinogen during fibrin production? | Chemotactic for neutrophils and enhancement of the effects of bradykinin |
| What is the function of the complement cascade? | Increased vascular permeability, chemotaxis, opsonization, and lysis of foreign organisms. |
| What of the 3 components of the Plasma Protease System is the most important? | Complement Cascade, because once activated, its components participate in practically every aspect of the inflammatory response. In addition, the last few compounds in the complement cascade (C5-C9 = MAC) are capable of killing microorganisms directly. |
| What activates complement cascade? | antigen-antibody complexes for the classical path and bacteria products or products of the other plasma protein systems for the alternative path. |
| Is complement a component of specific or non-specific immune defenses? | Non-specific (innate) |
| Activation of complement components C1 through C5 produces subunits which enhance inflammation in which ways? | 1) Opsonizing bacteria (C3), 2) Attracting leukocytes (Chemotaxis = C5a, C5b, C6, C7), and 3) by acting as mast cell degranulators for histamine release (C3a and C5a) |
| What do complement components C6 and C9 do? | Create pores in the bacterial walls producing influx of ions and fluid into bacteria which subsequently lyses. |
| What are the 3 ways in which inflammation can be classified? | 1) Duration, 2) Predominant type of the exudate formed, and 3) location in which the inflammation takes place and special forms |
| What is the difference in duration between acute and chronic inflammation? | Acute = less than 2 weeks, Chronic = 2 weeks or longer |
| Is chronic inflammation always the result of an unsuccessful acute inflammatory response? | No, only sometimes. Chronic inflammation can also occur without any prior evidence of acute inflammation = chronic from onset |
| What are the dominant pathological/anatomic features of acute inflammation? | changes in vasculature and exudate formation and grossly, cardinal signs |
| What is another name for acute inflammation? | Exudative inflammation |
| What are the dominant pathological/anatomic features of chronic inflammation? | Great amount of proliferation of cells and connective tissue (granulation/scar tissue) |
| When does acute inflammation become chronic? | After 2 weeks, if the injury cannot be resolved by acute inflammatory methods (ie – etiologic agent persists – such as peptic ulcer disease) |
| What are the 4 types of chronic inflammatory cells? | 1) Macrophages, 2) Lymphocytes (cell mediated/T-cells and humoral immunity/B-cells), 3) Plasma cells (humoral immunity), and 4) eosinophils (for parasitic infections and allergic reactions) |
| What are the two forms of chronic infection? | non-specific and granulomatous |
| Describe non-specific chronic inflammation. | Chronic inflammation in which there is no characteristic pattern of tissue reactions in which the participating cells are mononuclear (monocytes, lymphocytes, and plasma cells) and connective tissue cells (fibroblasts) |
| Describe chronic granulomatous inflammation. | Chronic inflammation characterized by a special tissue reaction that attempts to wall off and isolate the injurious agent. The participating cells are reticuloendothelial cells and their derivatives, largely macrophages. |
| What is usually (but not always) in the center of a granuloma? | Necrotic tissue (but sometimes it is a foreign body) |
| Describe the structure of a granuloma. | Central nodule surrounded by macrophages (usually modified to epithelioid cells) that are further surrounded by lymphocytes and/or plasma cells. Often, giant cells (multinucleate, of histiocytic or monocytic origin) are present among the inner cells. |
| What type of infection result in granuloma formation? | 1) TB (mainly), 2) Syphilis, 3) Cat Scratch Disease, 4) Fungal/Protozoan infections, 5) Foreign bodies (Tophaceous gout, pneumoconiosis = silica/asbestos), 6) Rheumatic fever (“Ashoff bodies”), 7) Rheumatic fever (subcutaneous nodules), 8) Sarcoidosis |
| Describe ‘Serous’ inflammation exudate. | 1) Usually due to mild injuries (blister burns, pulmonary TB, early bacterial infections), 2) only albumin-containing exudate, 3) derived from secretions of serosal mesothelial cells (peritoneal, pleural, pericardial, synovial) |
| Describe ‘Fibrinous’ inflammation exudate. | 1) More severe inflammation (vessels permitting passage of fibrinogen = exudate), 2) Characteristic of certain infections (Rheumatic fever = “Bread and butter pericarditis”, also in pneumoccoal pneumonias). Seen in both acute and chronic inflammation. |
| What happens to all the fibrin resulting from fibrinous inflammatory exudate formation? | It is removed via fibrinolysis or it gets replaced by fibrous scar tissue |
| What are the identifying features of serous inflammatory exudate in tissues? | Hard to identify, abnormally dilated spaces with fine precipitate of protein (albumin) |
| What are the identifying features of fibrinous inflammatory exudate in tissues? | Easy to identify because precipitated fibrin is deeply acidophilic, in strands and bands. |
| Describe Suppurative/Purulent inflammation exudate. | A type of liquefactive necrosis caused by pyogens (pus-producing bacteria) with the exudate containing lots of pus (protein rich fluid containing viable and necrotic neutrophils and tissue debris partially liquefied by proteolytic enzymes. |
| Which type of bacteria cause Suppurative/Purulent inflammation? | Pyogenic bacteria = 1) Staph, 2) Pneumococcus, 3) Meningococcus, 4) Gonococcus, 5) E. coli, 6) Non-haemolytic streptococcus |
| Give an example of a very common acute inflammatory process in which suppurative/purulent exudate would be seen. | Acute appendicitis |
| What are the identifying features of suppurative/purulent inflammation in tissues? | Pools of numerous PMNs (viable and dead) |
| Describe Sanguinous inflammation exudate. | Exudate containing a large number of RBCs, always indicates serious damage of the vessels RBCs enter perivascular tissue), almost never pure, but rather, mixed form with another of exudate (usually purulent, fibrinous, or both) |
| Give examples of situations in which Sanguinous exudate would form. | Seen in TB (Sanguinous pleuritis) or reaction to tumor invasion (sanguinous pericarditis). |
| What are the identifying features of Sanguinous exudate in tissues? | Presence of RBCs |
| Are most inflammatory exudates pure? | No, they are rarely pure. Often they represent a combination of two or more types of exudates (example = serosanguinous, fibrinopurulent, etc) |
| What is an ‘Abscess’? | Special form of inflammation = localized collection of pus caused by suppuration in tissue/organ. It is caused by an irritant of great intensity (Staphylococcus, Turpentine, etc) that characteristically remains localized, leading to great numbers of PMNs. |
| In abscess, what enzyme overcomes its inhibitor and causes digestion of damaged and dead tissue and converting it into a semisolid mass? | Trypsin (located liberated in situations of abscess) |
| What is a ‘Paronychia’? | Special form of inflammation seen when infection extends around the side and based of a fingernail. It is a rather painful and disabling lesion. |
| What is a ‘Felon’? | Special form of inflammation = a deep-seated infection in the anterior portion of the distal phalanx of of a finger (usually secondary to a penetrating wound). Felons may lead to osteomyelitis. |
| What is an ‘Empyema’? | Special form of inflammation = localized collection of pus in the plural cavity. |
| What is an ‘Ulcer’? | Special form of inflammation which is a local defect or excavation of the surface of an organ covered or lined by an epithelium (mucous membrane or epidermis) that produces sloughing of inflammatory necrotic tissue on or near the surface. |
| What is ‘Pseudomembranous inflammation’? | Special form of inflammation produced by powerful necrotizing toxin (ie - diphtheria) characterized by formation of pseudomembrane over the affected area. False membrane = Precipitated fibrin, necrotic epithelium, and WBCs. Occurs on mucosal surfaces. |
| What locations are typically affected by pseudomembranous inflammation? | Larynx, pharynx and other respiratory/GI passages. It occasionally occurs in the intestine of people taking antibiotics. |
| What is a ‘Fistula’? | An abnormal communication/opening (that isn’t always due to inflammation, it may be congenital or produced by tumor invasion) between two hollow organs lines by endothelium (ie – arteriovenous) or an epithelium (vesciouterine, vesciovaginal, etc) |
| What is a ‘Sinus’? | An abnormal communication/opening between a solid organ/tissue to an epithelium covered surface (usually skin), which may be caused by abscess burrowing from deep tissues. Unlike a fistula, this is usually caused by an inflammatory process. |
| What is ‘Bacteremia’? | Microorganisms circulate in blood but the patient does not appear to be ill (no fever, chills, etc) |
| What is ‘Septicemia’? | Bacteremia associated with clinical manifestation of illness: fever, chills, increased sedimentation rate, evidence of secondary seeding of organs (abscesses) |
| What is ‘Toxemia’? | Occurs when clinical illness is due to the presence of bacterial toxins in the blood, rather than bacteria. There are usually toxic changes in distant organs. |
| Describe the role of lymph and lymph nodes in resolution of inflammation. | Filtration/policing of extravascular fluids. Inflammation = lymph flow increases to decrease edema. Instead of collapsing, lymph channels actually open up due to a system of fibrils attached at right angles to thin walls which extend into adjacent tissue. |
| Is only fluid removed when lymph flow increases in an area of inflammation? | No, leukocytes and cell debris may also drain into lymphatic channels. |
| What is lymphangitis? | Inflammation of lymphatic channels |
| What is lymphadenitis? | Inflammation of a lymph node |
| What is the first, middle, and final stops in the flow pattern of lymphatic fluid? | First = lymph nodes, second = general circulation, final = Reticuloendothelial system (spleen) |
| What is bone marrow depression? | Disorder in which there are fewer circulation cells |
| What disorders are associated with defects in leukocyte adherence? | 1) Diabetes, 2) Acute alcohol intoxication, 3) corticosteroid therapy, 4) leukocyte adhesion deficiency |
| What are some *intrinsic* defects in leukocyte migration and chemotaxis? | 1) Chediak Higashi syndrome, 2) Lazy leukocyte syndrome, and 3) diabetes |
| Describe Chediak Higashi syndrome. | Microtubule polymerization defect in which the phagosome cannot fuse with the lysosome (also results in albinism and peripheral neuropathy). One will see ‘giant inclusion bodies’ within phagocytes under the microscope. |
| Describe Lazy Leukocyte Syndrome. | Severe neutropenia (low number of neutrophils) with associated abnormal neutrophil motility. |
| What are some *extrinsic* defects in leukocyte migration and chemotaxis? | 1) C5 deficiency, 2) Serum chemotactic inhibitors (C5 inactivators – especially in cirrhosis and sarcoidosis), 3) inhibitors of leukocyte locomotion, 4) drugs, 5) factors in malignancy, and 6) rheumatoid arthritis |
| How does diabetes affect opsonization? | Decreased opsonization due to Ig deficiency. |
| Which 3 defects are associated with reduced bacteriocidal activity? | 1) Chronic granulomatous disease (deficiency in NADPH oxidase = impaired H2O2 production), 2) Myeloperoxidase (MPO) deficiency, 3) severe G6PD deficiency |
| What causes redness? | Vasodilation by chemical mediators, particularly prostaglandins |
| What causes swelling? | 1) Exudation of fluid (edema), 2) breakdown of tissues, 3) mediation by C3a/C5a, bradykinin, and leukotrienes C, D, and E. |
| What causes heat? | increased blood flow, possibly increased local metabolic rate |
| What causes impaired function? | Swelling, inhibition of muscular contraction by pain |
| What causes pain? | Signaling of the neural system by chemical mediators (bradykinin, histamine, 5-OH-tryptamine |
| What causes fever? | Pyrogens (bacterial, chemical, endogenous substances from PMNs and other phagocytes). This includes prostaglandins. |
| What is leukocytosis? | Increase in the numbers of circulating WBCs often with immature forms What are the systemic effects of inflammation? |
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stephanieprater
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